Hostile behaviors predict cardiovascular mortality among men enrolled in the Multiple Risk Factor Intervention Trial.

BACKGROUND: Hostility is associated with incident coronary disease in most large population-based studies, but little is known about its association with cardiovascular disease (CVD) mortality in high-risk individuals. The aim of this study was to assess the association of hostility with CVD mortality in the subsequent 16 years in the Multiple Risk Factor Intervention Trial (MRFIT) participants and to explore the influence of hostility in the subset that had a nonfatal CVD event during the trial. METHODS AND RESULTS: We coded the Structured Interview responses of 259 men who died of CVD during the 16 years of follow-up and 259 matching living control subjects. Signs of hostility were assessed by use of the Interpersonal Hostility Assessment Technique. Matching was based on center, intervention group, age, race, and interviewer; covariates included study entry diastolic blood pressure, cholesterol, smoking status, and nonfatal CVD event during the trial. High-hostile men were more likely to die of CVD than were low-hostile men. Adjusted odds ratio (OR) and 95% confidence intervals (CIs) were 1.61, 1.09 to 2.39. After the trial, high-hostile men who also had a nonfatal event during the trial were particularly likely to die of CVD, OR, 5.06, 1.42 to 8.22, compared with low-hostile men without a nonfatal event during the trial. CONCLUSIONS: Hostility may be a risk factor for CVD mortality among high-risk men. Interventions aimed at anger management and stress reduction along with risk factor modification may be useful for hostile patients.

Influence of hormone therapy on the cardiovascular responses to stress of postmenopausal women.

Epidemiological and psychophysiological data suggest that groups that differ in reproductive hormones and stress responses also differ in risk for cardiovascular disease. To evaluate the effects of hormone therapy on women's cardiovascular responses to laboratory stressors, 89 healthy postmenopausal women were tested twice, before and after exposure for about 8 weeks to one of the five conditions: placebo, Estratab (primarily estrone), Estratab plus Prometrium (micronized progesterone), Estratab plus Provera (synthetic progestin), and Estratest (same estrogen as in Estratab plus methyltestosterone). Results showed that women assigned to Estratab plus Prometrium and Estratest had diminished systolic blood pressure responses to stress upon retesting, whereas the other groups did not change in the level of their responses. Women assigned to Estratab plus Prometrium had diminished diastolic blood pressure responses during a speech stressor upon retesting, whereas women assigned to Estratab plus Provera increased. Our findings show that hormone therapy does affect women's stress responses, but they do not provide a simple explanation as to why groups at high and low risk for cardiovascular disease differ in reproductive hormones and stress responses.

Interactions between autonomic nervous system activity and endothelial function: a model for the development of cardiovascular disease.

OBJECTIVES: Endothelial dysfunction is a new pathway in cardiovascular disease (CVD) development. Psychosocial factors have been little studied in relation to endothelial function, although they may interact via associations with the autonomic nervous system (ANS). The purpose of this review is to propose a model by which psychosocial factors are related to CVD development through interactions between the ANS and vascular endothelium. METHODS: The literature supporting an interaction between the ANS and endothelium in healthy and disease states is reviewed. Potential mechanisms linking the two systems are explored as a pathway for CVD development. RESULTS: Endothelial dysfunction and impaired cardiovascular ANS regulation are both markers for increased CVD risk. Sympathetic nerves and vascular endothelial cells share a functional antagonism in healthy states to maintain appropriate blood vessel tone. Alterations in sympathetic activity and endothelial cell function are both observed early in the development of CVD and may result from an inability to maintain the functional antagonism. Impairments in either ANS regulation or endothelial function may contribute to further disease development by evoking maladaptive changes in the opposing system. CONCLUSIONS: Although interactions between cardiovascular ANS regulation and endothelial function are likely involved in CVD development, further research is needed to determine whether ANS and endothelium interactions are a plausible pathway linking psychosocial factors with increased CVD risk.

Associations between psychological traits and endothelial function in postmenopausal women.

OBJECTIVE: The objective of this study was to determine whether psychosocial risk factors for cardiovascular disease (CVD) are associated with impairments in endothelial function and to determine whether use of hormone replacement therapy (HRT) can moderate observed associations among women without prior CVD. METHODS: Flow-mediated dilation was assessed by brachial ultrasound after reactive hyperemia in 193 postmenopausal women enrolled in the prospective Healthy Women Study. Measures of psychosocial characteristics had been completed at study entry, when the women were premenopausal (mean = 13.6 years earlier), and at a separate postmenopausal follow-up exam near the time of the ultrasound (mean = 1.5 years earlier). RESULTS: Factor analyses of the psychosocial characteristics yielded two factors: Type A/anger and anxiety/depression. Anxiety/depression scores at the study entry and follow-up exams and Type A/anger scores at the study entry exam were associated with less vasodilation (p values < 0.05). Type A/anger scores at the follow-up exam were associated with less vasodilation among women not using HRT (p <.05). CONCLUSIONS: Psychosocial risk factors for CVD are associated with impaired brachial artery dilation among postmenopausal women. HRT use may mask some associations between psychosocial risk factors and endothelial dysfunction among postmenopausal women.